bronchoalveolar lavage fluid from rats

Significant differences inseveralcomponents of bronchoalveolar lavage fluid (BAL fluid) have previously been reported in aluminium potroom workers compared with controls. The present paper describes the long term effects in rats of one time exposure to potroom aluminium oxide without fluorides (primary alumina (PA)) or with adsorbed fluorides (secondary alumina (SA) ) on components of BAL fluid. Alumina dust (40 mg) suspended in saline was instilled intracheally; controls received saline. Bronchoalveolar lavage (BAL) was performed one, four, and 12 months after exposure. The number of cells in BAL fluid was increased significantly (p < 0 05) by SA but not PA. The increase was mainly macrophages, but the concentrations of neutrophils also increased about 10-fold one and 12 months after exposure. Although albumin and hyaluronan concentrations did not differ from those of controls, fibronectin concentrations were significantly (p < 0-001) increased one year after exposure both in PA exposed and SA exposed rats. The results indicate that SA, possibly because of adhered fluorides, induces early changes in alveolar cell populations including persistent neutrophilia. These cellular changes may have a destructive effect. The late pronounced increase of fibronectin in both PA and SA exposed rats indicates a delayed effect of alumina on the extracellular matrix. (British Journal of Industrial Medicine 1993;5O:172-175) According to the review by Abramson et all aluminium reduction plant employees may develop an asthmatic syndrome, chronic obstructive lung disease, lung cancer, or pulmonary fibrosis. More recent reports, however, have failed to find clinical and British Journal of Industrial Medicine 1993;50:172-175 physiological signs of significantly impaired lung function in such workers.`3 Potroom workers are exposed to two kinds of dust particles; "pure" alumina (aluminium oxide, Al,03) and alumina with adhered gases, mainly fluorides. It is generally believed that pulmonary fibrosis is caused by the aluminium oxide, whereas potroom asthma has been attributed to irritants other than alumina such as fluorides.' 4 Early histopathological studies on alumina exposed rats (see review5) have shown that only the intratracheal instillation of reactive transitional alumina and high surface area alumina induced a fibronodular response. No clear cut fibrogenic effect was produced by "industrial" alumina. The BAL fluid response of alumina exposed rats was an early, and rapidly receding, increase in macrophages, lymphocytes, and polymorphonuclear cells,67 total protein concentration, and activity of cytolytic enzymes.7 Histologically, a transitional granulomatosis but no fibrosis was found.6 In vitro, crystalline particulate aluminium hydroxide showed no harmful effects on macrophages and fibroblasts.' Using BAL for the examination of aluminium potroom workers, we have reported9 significant changes in several components compared with controls despite an absence of clinical symptoms. Thus it seemed that even mild prolonged exposure to pollutants in the potrooms may affect the alveolar environment. The findings prompted our present study on the long term effects of specific industrial samples of alumina in rats. To detect the possible influence of fluoride, effects of potroom aluminium oxide without (primary alumina (PA) ) and with adsorbed fluorides (secondary alumina (SA) ) were compared. Besides markers of inflammatory alveolar reactions, two soluble components of the extracellular matrix were measured to trace possible fibrogenic effects.